Jackie Christensen was 32 when her body began to betray her. She had just returned to work after the birth of her second son and when she tried to type, two fingers on her left hand refused to cooperate. “They wouldn’t go where I would want them to on the keyboard,” says Christensen, who at the time — it was 1997 — was co-director of the food and health program at the Institute for Agriculture and Trade Policy, a Minneapolis think tank. “I also had what they frequently call frozen shoulder, with a very low range of motion in my left arm.”

The first neurologist Christensen went to responded flippantly to her suggestion that she might have multiple sclerosis, which she had self-diagnosed because of her relatively young age and the fact that she was female. “If you want me to write that down, I will,” she remembers him saying, refusing to pursue the matter further. A second neurologist thought it was all in Christensen’s mind and referred her to a psychiatrist. Over the next several months, her symptoms got progressively worse, and she finally consulted neurologist number three. His startling diagnosis: Parkinson’s disease.

“I thought, ‘I can’t have Parkinson’s because I’m not old,'” Christensen recalls. But a trial of the standard treatment, a drug called L-dopa, seemed to work. Based on that clinical observation, the diagnosis was confirmed. This was in 1998, when Christensen was not quite 35, and she has been on L-dopa, with varying degrees of success, ever since.

Why did a disease that usually affects people in their sixties and seventies, and that affects men more often than women, strike this vibrant young mother? Christensen, a lifelong environmental activist, suspected an environmental cause — not only because she was politically inclined to, but because she knew that accumulating scientific information was pointing in that direction. In the past few years, Christensen has been part of a movement exploring a possible connection between exposure to environmental toxins — in particular, the organophosphate pesticides — and Parkinson’s disease, through her work with the Collaborative on Health and the Environment, a national network of advocacy and scientific organizations. She is co-founder of CHE’s working group on Parkinson’s Disease and the Environment.

A cause-and-effect relationship between environmental neurotoxins and Parkinson’s is difficult to prove. As with many other scientific efforts to establish disease causation through population studies, there will probably never be a smoking gun that settles things once and for all. Population studies can detect associations between certain suspected agents and diseases such as cancer, but it’s hard to draw conclusions about what causes a disease from studies that can register only correlations. In the case of Parkinson’s and the environment, however, there has been a steadily mounting consensus about such a connection, and the pace has quickened in the past year or so.

A January 2009 consensus statement from CHE, in collaboration with the Parkinson’s Action Network, a patient advocacy group, found that there was “limited suggestive evidence of an association” between pesticides and Parkinson’s, and between farming or agricultural work and Parkinson’s. This followed by just a few months the publication of Environmental Threats to Healthy Aging, a report co-authored by the Science and Environmental Health Network, a consortium of advocacy groups based in Ames, Iowa; it included a summary of 31 population studies that have looked at the possible connection between pesticide exposure and Parkinson’s. Twenty-four of those studies, according to the report, found a positive association, and in 12 cases the association was statistically significant. In some studies, the group found, there was as much as a sevenfold greater risk of Parkinson’s in people exposed to pesticides. In addition, in April 2009, scientists at the University of California, Los Angeles published a provocative study connecting the disease not only to occupational pesticide exposure but also to living in homes or going to schools that were close to a pesticide-treated field.

Taken together, 30-plus years of research add up to an increasingly persuasive conclusion: exposure to pesticides and other toxins increases the risk of Parkinson’s disease, and we are only now beginning to wrestle with the true scope of the damage.

Parkinson’s is the second most common neurodegenerative disease (after Alzheimer’s) in the United States, affecting between 1 million and 1.5 million Americans. The majority of cases occur in people over 65, about 60 percent of them male. It leads to uncontrollable tremors, muscle rigidity, and the inability to direct your arms or legs to move when you want them to. People with Parkinson’s often have a masklike, impassive expression. They may have difficulty speaking clearly and develop a characteristic shuffling gait. Cognitive skills usually are not affected, though some functions like memory and decision-making can be impaired, and, in the face of the gradual and inevitable encroachment of physical limitations, people with Parkinson’s often become depressed.

In part because it can take many forms, Parkinson’s disease is difficult to diagnose. Several movement disorders have been classified in the general category known as Parkinson’s-like syndrome, or parkinsonism. Scientists are divided about whether Parkinson’s disease and parkinsonism are even related in any meaningful way, beyond sharing some symptoms. The two conditions may not even involve the same brain defects. The strict definition of Parkinson’s disease is a loss of cells in the substantia nigra, a small structure in the basal ganglia region of the midbrain (though other brain structures are now thought to be involved as well). The substantia nigra ordinarily secretes the neurotransmitter dopamine, which is involved in many of the brain’s functions, including the control of motor activity.

Often a diagnosis of Parkinson’s disease is made the way it was made for Christensen: by a trial run of L-dopa, which boosts dopamine in the brain. If it works, the problem must be Parkinson’s. It’s a circular kind of logic, but it’s all that most doctors have. There still are no definitive blood tests or brain scans to make the diagnosis.

“Despite remaining uncertainties and data gaps,” wrote the authors of a 2008 report by the Science and Environmental Health Network — Jill Stein, Ted Schettler, Ben Rohrer, and Maria Valenti — “the body of evidence linking pesticide exposure to Parkinson’s disease fulfills generally accepted criteria for establishing causation.” When combined with “extensive laboratory animal data” specifying the underlying biology of this relationship, they wrote, “collectively, this evidence supports the conclusion that pesticide exposures can cause Parkinson’s disease in some people.”

Like most other population studies, this one has no way of proving that, for any one individual, X definitely led to Y — that Jackie Christensen’s early-onset Parkinson’s disease, for instance, was caused by her exposure to pesticides as a teenager. To Christensen, however, the causal connection is clear. Growing up in rural Minnesota, she spent summers working on local farms. In her early teens, this meant engaging in a practice known as “walking beans.” A pickup truck would drop off a bunch of youngsters, including Christensen, at one end of a field, and they would walk the rows of soybeans, weeding as they went. Later, Christensen and her friends rode a “bean buggy,” a rig attached to the front of a tractor from which they would spray the herbicide Roundup, sometimes dyed purple so they could see where it was landing, carefully aiming for the weeds and trying to avoid the beans. Often she was dressed in nothing more than a bathing suit and a baseball cap. “I had a great tan those summers,” she wrote in the introduction to her book, The First Year: Parkinson’s Disease; An Essential Guide for the Newly Diagnosed, “and I had no idea nor gave any thought whatsoever to what I might be exposing myself to, or what the effects might be. After the first day or two of spraying, I could no longer smell the odor of the herbicide. I do remember that when I would come home, my mother would immediately tell me to take a shower because I smelled like chemicals.”

As a young adult, Christensen had a single massive chemical exposure, during a political demonstration that involved wading into the Mississippi River in St. Louis. Wastewater treatment runoff made the water as neon green as Mountain Dew. She says it’s “anybody’s guess” what was in the water, but since many of the industries in St. Louis at the time discharged their wastes into the river, she says the brew probably included organophosphate pesticides, dry cleaning solvents, and other compounds. “After that action, within an hour I had a headache,” she says, “and I was nauseated and felt fatigued and lousy for a week. I know now that those are common symptoms of acute pesticide poisoning. At the time I didn’t think about what was causing it. I was 25 and thought I was bulletproof.”

Since the British physician James Parkinson first described the “shaking palsy” in 1817, Parkinson’s disease has been linked to a variety of possible environmental causes, both natural and artificial. It has been linked, too, to genetic factors, dating back to the beginning of the twentieth century, when early-onset Parkinson’s was first found to run in a few scattered, unlucky families. Those who study the connection between Parkinson’s and the environment suggest that it’s probably the combined result of having a genetic predisposition to the disease and a dangerous exposure to some sort of neurotoxin. A favorite expression of people in this field is that “genetics loads the gun and environment pulls the trigger.”

Robin Marantz Henig is a contributing writer to the New York Times Magazine. She is the recipient of a 2009 Guggenheim Foundation fellowship, and is the author of eight books on science, including The Monk in the Garden (Houghton Mifflin), a finalist for the National Book Critics Circle Award.

Usually the old has a Parkinson.Why does this case is only 32 years old?

Lilly Walcott

The disease of Parkinson is a neurodegenerativo process of the extrapiramidal system that approximately affects 1% of the greater people of 50 years. The Parkinson was discovered for the first time by the English doctor James Parkinson in 1817. Between his more important clinical characteristics it appears depression, anxiety, muscular rigidity, slowness in the corporal movements, the postural instability and the face inexpressiveness.

Causes:

The disease of Parkinson this caused by the death or deterioration of certain neurons, in an area of the well-known brain like substance nigra. These neurons produce dopamine, the neurotransmitter in charge to transmit signals between the substance nigra and corpus striatum, being mediated therefore a good muscular activity.

The reduction in the dopamine production causes in the patients and incapacity to direct or to control its movements of normal form, had al uncontrolled of the nervous cells of striatum. The studies have demonstrated that the patients of Parkinson have a loss of 80% or more of the producing dopamine cells in the substance nigra. The cause of this death or cellular deterioration is not known.